Position statement
Posted: May 26, 2026
Justin Penner MD, Sergio Fanella MD; Canadian Paediatric Society, Infectious Diseases and Immunization Committee
Skin and soft tissue infections (SSTIs) are among the most common infectious diseases encountered in children. Severity of SSTIs range from simple infections that resolve spontaneously to severe necrotizing syndromes requiring intravenous antibiotics, surgical intervention, and intensive care. Inadequate skin barrier resulting from common paediatric conditions such as eczema and skin abrasions predisposes to infection. When antibiotics are needed, their choice and duration should be guided by the most probable organisms involved, their likely susceptibility profiles, and geographical epidemiologic differences. Inappropriate treatment with overly broad-spectrum antibiotics and/or for prolonged durations is detrimental to the microbiomes of patients, increases antimicrobial-related side effects, and perpetuates colonization of resistant organisms, precipitating antimicrobial resistance. This statement provides health care providers with a toolkit for optimal management of bacterial SSTIs, including recurrent episodes. It does not comprehensively examine SSTI treatment principles in immunocompromised or burn patients due to the management complexities of both settings.
Keywords: Abscess; Cellulitis; Decolonization; MRSA; Skin infection
The skin protects its host from infection by acting as a physical barrier. Damage to this barrier from a variety of processes, including atopic disease, skin irritants, xerosis, micro abrasions, ectoparasites (e.g., scabies, lice), trauma, surgery, viral skin infections (e.g., herpes-zoster/herpes simplex [HZV/HSV]), or hair/nail infections, increases vulnerability to infection.
Skin and soft tissue infections (SSTIs) are some of the most common infectious diseases encountered in paediatrics. A Canadian multicentre study of 12 remote/isolated communities estimated the prevalence of SSTIs in some sites at 36.8%, with 60.2% of the total population studied having received at least one antibiotic prescription in the preceding 12 months[1]. Such high antimicrobial use may be linked to higher rates of antibiotic-resistant infections in these communities. Both the frequency of SSTIs in the paediatric population and the potential for high antimicrobial use resulting in infections with resistant organisms make antimicrobial stewardship a public health issue of paramount concern. This statement provides health care providers with a toolkit for optimizing the management of bacterial SSTIs, including recurrent episodes. It replaces previous guidance on methicillin-resistant Staphylococcus aureus (MRSA) skin abscesses from the Canadian Paediatric Society[2].
SSTIs have been categorized in various ways, without universal consensus. A list of common terms can be found in Table 1. Bacterial infections of the epidermis are typically less severe than deeper infections, but they can facilitate bacterial entry into deeper tissues. Abscesses can manifest in any of the tissue layers and are characterized by discrete collections of pus (Figure 1).
Table 1. Skin and soft tissue infections: Terms and definitions*
Figure 1. Skin and soft tissue infection anatomy

Delays in initiating treatment and inconsistencies in management practices can cause disease progression, pain, deep-tissue abscesses, musculoskeletal infections, and hypo- and hyperpigmentation. Inappropriate antibiotic initiation, duration, and drug or route selection for simple infections are detrimental to the individual’s microbiome, increase antimicrobial-related side effects (e.g., Clostridioides difficile), and have societal impacts through increased antimicrobial resistance.
The most common pathogens associated with community-acquired bacterial SSTIs include methicillin-susceptible or -resistant Staphylococcus aureus (MSSA or MRSA) and Streptococcus pyogenes (Group A Streptococcus [GAS]). Both pathogens can cause a range of SSTIs, from mild infections (e.g., folliculitis, impetigo) to severe necrotizing infections complicated by toxic shock or sepsis. Recent reports have suggested an increase in invasive GAS infections[3]. Non-pyogenic cellulitis has been reported more with GAS compared with S. aureus, although microbiological confirmation is rare in this context and Canadian data is lacking in paediatric populations[4].
Although variable by province/territory, an increase in paediatric MRSA has been recognized in Canada[5][6]. This rise disproportionately impacts certain minoritized groups, such as Indigenous communities in remote/isolated areas, where MRSA proportions can exceed 50%[7]. Such prevalence indicates that certain social determinants of health, such as crowded housing, are risk factors for SSTIs[8]. Colonization rates of up to 67% have been reported in households where one member has had a recent MRSA infection[9]. Certain behaviours, such as nose-picking, have been associated with increasing rates of S. aureus carriage[10][11]. Some studies have shown that approximately one-third of individuals colonized with MRSA will develop an SSTI[12][13], and up to 70% with an MRSA SSTI may experience recurrence(s) over the following 6 to 12 months[14]. SSTI risk in children also increases with MSSA colonization[15].
Other bacterial pathogens and non-infectious mimics should be considered based on exposure history and examination. Waterborne pathogens include Aeromonas spp (in fresh water), Vibrio spp (in brackish or salt water), and Pseudomonas aeruginosa (causing hot tub folliculitis, or ecthyma). Anaerobic bacteria can cause SSTIs following a deep puncture wound or animal or human bite, and may feature in cases of longstanding ulcerative lesions, immunocompromised hosts, and prolonged or recent antimicrobial use. Consider non-tuberculous mycobacteria, candida, moulds, and cutaneous dermatophytes when the epidemiology or morphology of lesions suggests such etiologies. VZV infections predispose to SSTIs, including invasive infections (e.g., necrotizing fasciitis)[16]. Eczema can also be superinfected with HSV (eczema herpeticum) or enteroviruses (eczema coxsackium). Non-infectious mimics of SSTIs include, but not limited to: pyoderma gangrenosum, pyogenic granuloma, psoriasis, non-infected atopic dermatitis, hidradenitis suppurativa, venous stasis or thrombosis, vasculitis, urticaria, contact dermatitis, malignancy, and other non-infectious dermatologic or rheumatologic conditions.
The epidemiological triad comprises the host, pathogen, and environment. A focused history should consider interactions among the three, including preceding skin trauma, bites (animal or human), water exposures, travel, sick contacts, social, occupational, and recreational activities, and hospitalization(s) or frequent health care admissions or attendance. Chronicity (i.e., acute, subacute, or chronic) and associated symptoms (i.e., fever, pain) should form part of an SSTI history. Past medical history should include personal and family experience of previous SSTIs, underlying medical conditions, known history or risk factors for MRSA colonization, and vaccination status. While most children with recurrent SSTIs are immunocompetent, a careful history should ensure there are no “red flags” for inborn errors of immunity, such as recurrent, invasive, multi-site, or unusual infections, early age of onset, deep skin or lymph node abscesses, failure to thrive, and severe or intractable eczema. In cases of recurrent perianal abscesses, inflammatory bowel disease should be considered.
Severity assessments are largely subjective, though scoring systems have been validated to help define mild, moderate, and severe disease. One scoring system for cellulitis is the Melbourne ASSET score. Higher scores suggest increasing severity, with a cut-off of 4 limiting unnecessary intravenous (IV) antibiotics[17]. In a case-based survey of paediatricians, the most common findings associated with severity and treatment with IV versus oral antimicrobials included tracking lymphangitis, functional impairment of the affected area, fever, oral antibiotics within the previous 24 hours, size, site, and degree of swelling and tenderness[18]. Further findings suggestive of severe invasive disease include pain out of proportion to clinical findings, rapidly expanding erythema, necrosis, and crepitus.
Microbiological samples should be sought for open wounds or lesions with visible pus or fluid. Pus collected by needle aspirate, surgical, or manual drainage of abscesses should be cultured and prioritized over swabs based on their higher microbiological yield. Superficial swabs of intact and non-intact skin or ulcers are of limited use due to isolation of colonizing microbiota. If debridement is indicated, tissue samples for culture are of highest yield. Other samples (e.g., skin biopsy) may be considered in settings of chronic infection, failed therapy, an immunocompromised child, or unusual exposure(s). In such cases, an infectious disease (ID) or dermatology consult (or both) should be sought to guide specimen requests. Specialized viral swabs from deroofed vesicles placed in dedicated media are warranted for HSV, VZV, and enterovirus polymerase chain reaction (PCR) testing. Blood cultures are rarely indicated with clinically mild to moderate SSTIs but should be collected with systemic illness, shock, and severe or deep-seated infections. Dermatophyte and ectoparasite skin scrapings should be collected when clinically indicated, following local laboratory protocols.
(Figure 2)
Clinicians should first consider whether antimicrobials are warranted. Minor infections can resolve spontaneously with wound care alone. Best practices for wound care management can be found at woundscanada.ca. In addition to wound care, a short-course prescription (3 to 5 days) of topical antimicrobials may be required. Evidence of benefit for over-the-counter topical antimicrobials (e.g., polymyxin B, bacitracin, neomycin) is unclear[19]. Empiric antimicrobial choices should be individualized based on history (e.g., exposures), examination findings, and previous microbiology results when available. More recent microbiological results should be prioritized. Local paediatric-specific antibiograms are encouraged to help guide empiric antimicrobial choice.
Empiric antibiotics should target the most common pathogens causing SSTIs (Table 2[20]-[22]) and most infections are amenable to oral treatment. In the majority of cases, including moderate infections, oral cephalexin is appropriate, provided that adequate dosing is administered[23]. Combination therapy with cephalexin and trimethoprim/sulfamethoxazole or broad-spectrum outpatient IV antibiotics (e.g., ceftriaxone) are discouraged. Empiric therapy targeting MRSA may be warranted in some cases, such as when children are colonized or living in MRSA-prevalent areas (i.e., where >10% to 15% S. aureus isolates are MRSA)[24]. Oral trimethoprim/sulfamethoxazole is preferred due to high susceptibility rates for MRSA in Canada. Clindamycin resistance is higher, although this antibiotic may still be considered for children with prior susceptible isolates or when antibiograms demonstrate high susceptibility. When a patient is known to be carrying MRSA (e.g., MRSA-positive nares) or later found to be after initiating antimicrobials but has improved with non-MRSA treatment, switching antimicrobials is not necessary. For children colonized with MRSA or living in highly MRSA-endemic areas and presenting with a non-purulent SSTI (e.g., cellulitis) without systemic features, consider initiating a non-MRSA antimicrobial (e.g., cephalexin) with close follow-up[25][26].
For hospitalized children, antimicrobial choice is guided by the history and severity of disease. For non-toxic children who have not been exposed to atypical pathogens, IV cefazolin or, when MRSA is suspected, vancomycin, is appropriate. For children who are systemically unwell or toxic (e.g., concern for sepsis, fasciitis/myositis, shock), many experts recommend initiating broad-spectrum coverage (ceftriaxone or piperacillin-tazobactam, plus vancomycin) empirically, then discontinuing vancomycin when MRSA is excluded. The addition of an anti-toxin antibiotic (e.g., clindamycin) should be strongly considered in such cases[27]. ID consultation should be sought and antibiotics targeted to microbiology results. When SSTIs are complicated by a herpesvirus (e.g., HSV/VZV), IV acyclovir or oral acyclovir/valacyclovir may be warranted.
Table 2. Antimicrobials for treating systemic skin and soft tissue infections (SSTIs)
* Dose adjustments may be required based on hepatic/renal function or for infants. Consult with pharmacy as required.
† Low risk: <10%–15% S. aureus isolates are MRSA; High risk: >10%–15% S. aureus isolates are MRSA GAS Group A streptococcus; IV Intravenous; MRSA Methicillin-resistant Staphylococcus aureus; MSSA Methicillin-susceptible Staphylococcus aureus; TMP/SMX Trimethoprim/sulfamethoxazole
Source control of abscesses through surgical or manual drainage is vital. Warm compresses can facilitate drainage. When drainage of an uncomplicated small collection is achieved in a healthy host, without significant surrounding cellulitis, antimicrobials are rarely warranted[28]-[30]. If antimicrobials were started previously, they can typically be discontinued when drainage is achieved. Post-drainage wound care is important for healing and consultation with experts in wound care may be considered.
In cases of necrotizing infection, urgent surgical consultation for debridement is essential. Deep samples of pus and tissue should be sent for aerobic and anaerobic cultures. Debridement of chronic ulcers and biopsies of unusual or chronic lesions and those failing therapy ensures that tissue can be sent for bacterial, mycobacterial, and fungal cultures and for histopathology to aid diagnosis and targeted therapy.
Figure 2. Treatment algorithm for skin and soft tissue infections (SSTIs)

* Abscess, carbuncle, furuncle
† Mild infection (small area): Systemically well, localized SSTI, no or minimal erythema or induration, no deep-seated infection. Outpatient treatment. May resolve with appropriate skin care alone
‡ Moderate infection (e.g., limited cellulitis): Systemically well, not rapidly progressive, no deep-seated infection. Outpatient treatment
§ Severe infection (e.g., widespread cellulitis/deep-seated infection): Extensive infection, clinically unstable, rapidly progressive, necrosis, pain out of proportion, crepitus. Inpatient treatment. If systemically unwell, start empiric antibiotics urgently
¶ Re-evaluate diagnosis (repeat history/examination), need for source control
** Consult ID, refer to local antimicrobial guidelines
‡‡ MRSA risk factors: MRSA colonized, previous or recurrent MRSA SSTIs, local prevalence >10% to 15%
ID Infectious diseases; IV Intravenous; IVIG Intravenous immunoglobulin; MRSA Methicillin-resistant Staphylococcus aureus
Preserving an intact skin barrier, including wound management and control of primary dermatologic disorders, is important to prevent SSTIs, including recurrence. Optimize eczema management, including breaking the pruritus→scratch→skin breakdown cycle. Dermatology consultation should be considered for children with difficult-to-control skin conditions that threaten recurrence or serious infection.
In healthy patients, decolonization has achieved mixed results in preventing SSTI recurrence, and treatment regimens and practices vary with no clear consensus[31]-[36]. Decolonization practices can also be costly and dry the skin if concurrent moisturizers are not used. Recurrence of colonization is common, even with diligent decolonization practices[37]-[39]. Some experts reserve decolonization for recurrence of moderate to severe SSTIs, household outbreaks, or to prepare for procedures with high infection risk. Challenging cases often benefit from ID consultation, and the advantages and disadvantages of treatments and their variable success rates should be discussed with families. When recommended, a 5-day trial of 2% mupirocin ointment twice daily to nares, combined with daily cleaning with 4% chlorhexidine soap or 2% chlorhexidine wipes (for 5 to 7 days) is suggested[40]. Dilute bleach baths (DBBs) are an acceptable alternative and can be used as part of both decolonization regimens (daily for 5 to 7 days) or maintenance suppression (or both)[41]. Concurrent family/household member decolonization may also be considered to increase chances of decolonization success, although evidence for this practice is inconsistent[42]-[44]. Use of oral antimicrobial agents for decolonization is discouraged unless directed by ID[31].
DBBs are prepared with 1/4 to 1/2 cup bleach added to a bathtub of water. Children should be encouraged to sit in the bath for 5 to 10 minutes. Swimming in a chlorinated pool has similar effect. Maintenance DBBs for children with a recurrent SSTI may be continued once or twice per week to suppress bacterial microbiota. Make sure that skin moisturizer is being applied after bathing. Concurrent environmental decolonization measures in the household include cleaning surfaces with bleach-containing solution, focusing on “high-touch” surfaces, washing towels, clothing, and bedding in hot water, and replacing or disinfecting personal hygiene items[45]-[47]. Sharing such items and sharing athletic equipment are discouraged. To help maximize success, clinicians are encouraged to develop written handouts describing these regimens, including images, detailed instructions, with translation into local languages.
Additional measures to decrease recurrence include diligent wound care, covering open wounds, encouraging universal uptake of varicella vaccination, and regular cleaning of communal, sporting, and exercise equipment (ideally after each use). Scabies and lice predispose to SSTIs and should be treated per local guidelines[48][49]. Chronic antibiotic suppression is rarely indicated but may be considered in consultation with ID for certain inborn errors of innate immunity, chronic or recurrent dermatologic diseases, or conditions of aberrant lymphatic drainage.
This position statement was reviewed by the Community Paediatrics and First Nations, Inuit and Métis Health Committees of the Canadian Paediatric Society (CPS). It was also reviewed by the CPS Community Paediatrics, Hospital Paediatrics, and Paediatric Emergency Medicine Section Executives, and by members of the Association of Medical Microbiology and Infectious Disease Canada (AMMI).
CANADIAN PAEDIATRIC SOCIETY INFECTIOUS DISEASES AND IMMUNIZATION COMMITTEE (2024-2025)
Members: Michelle Barton MD (Chair), Laura Sauvé MD (Past Chair), Eugene Ng MD (Board Representative), Ari Bitnun MD, Jeannette Comeau MD MSc, Sergio Fanella MD, Justin Penner MD, MSc
Liaisons: Dorothy Moore MD (National Advisory Committee on Immunization), Ari Bitnun MD (Canadian Paediatric and Perinatal HIV/AIDS Research Group), Isabelle Viel-Thériault MD (Committee to Advise on Tropical Medicine and Travel), Marina Salvadori MD (Public Health Agency of Canada), Sean O’Leary (American Academy of Pediatrics, Committee on Infectious Diseases), Rupeena Purewal MD (Immunization Monitoring Program, ACTive), Cora Constantinescu MD (Association of Medical Microbiology and Infectious Disease Canada, Pediatric Committee)
Principal authors: Justin Penner MD, Sergio Fanella MD
Funding
There is no funding to declare.
Potential Conflict of Interest
Dr. Fanella reported receiving funding as a local site PI for MCT for COVID19 vaccines in children (ModernaTx). No other disclosures were reported.
Disclaimer: The recommendations in this position statement do not indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate. Internet addresses are current at time of publication.